Enhancement of endothelial cell migration by constitutively active LPA₁-expressing tumor cells

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• 作者：Misaho Kitayoshi^a ; Kohei Kato^a ; Eriko Tanabe^a ; Kyohei Yoshikawa^a ; Rie Fukui^a ; Nobuyuki Fukushima^b ; Toshifumi Tsujiuchi^a ; ^{ttujiuch@life.kindai.ac.jp}
• 关键词：LPA ; lysophosphatidic acid ; LPA1 ; LPA receptor-1 ; VEGF ; vascular endothelial growth factor ; RT ; reverse transcription ; PCR ; polymerase chain reaction
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：1 June, 2012
• 卷：422
• 期：2
• 页码：339-343
• 文件大小：550 K

摘要

Lysophosphatidic acid (LPA) receptors belong to G protein-coupled transmembrane receptors (LPA receptors; LPA₁ to LPA₆). They indicate a variety of cellular response by the interaction with LPA, including cell proliferation, migration and differentiation. Recently, we have reported that constitutive active mutated LPA₁ induced the strong biological effects of rat neuroblastoma B103 cells. In the present study, we examined the effects of mutated LPA₁ on the interaction between B103 cells and endothelial F-2 cells. Each LPA receptor expressing B103 cells were maintained in serum-free DMEM and cell motility assay was performed with a Cell Culture Insert. When F-2 cells were cultured with conditioned medium from Lpar1 and Lpar3-expressing cells, the cell motility of F-2 cells was significantly higher than control cells. Interestingly, the motile activity of F-2 cells was strongly induced by mutated LPA₁ than other cells, correlating with the expression levels of vascular endothelial growth factor (Vegf)-A and Vegf-C. Pretreatment of LPA signaling inhibitors inhibited F-2 cell motility stimulated by mutated LPA₁. These results suggest that activation of LPA signaling via mutated LPA₁ may play an important role in the promotion of angiogenesis in rat neuroblastoma cells.